title: Is hypertension an immunologic disease?
abstract: Several studies published in the past three decades have suggested that the adaptive immune system contributes to hypertension. Recent studies have shown that T cells play a crucial role in the blood pressure elevation caused by angiotensin II and in response to sodium and volume challenge. Hypertensive stimuli cause effector T cells to enter visceral fat, in particular perivascular fat, where they release cytokines that promote vasoconstriction. Similarly, effector T cells accumulate in the kidney in hypertension and contribute to renal dysfunction, promoting sodium and volume retention. These findings provide some insight into the relationship between inflammation and hypertension and suggest that efforts to reduce T-cell activation may be useful in preventing or treating this disease.
authors.affiliation: Department of Medicine, Division of Cardiology, Emory University School of Medicine, Room 319 WMRB, 1639 Pierce Drive, Atlanta, GA 30322, USA. dharr02@emory.edu
authors.forename: David G
authors.initials: DG
authors.lastname: Harrison
authors.forename: Tomasz J
authors.initials: TJ
authors.lastname: Guzik
authors.forename: Jorg
authors.initials: J
authors.lastname: Goronzy
authors.forename: Cornelia
authors.initials: C
authors.lastname: Weyand
mesh_terms: D001794:Blood Pressure; D016207:Cytokines; D006801:Humans; D006973:Hypertension / Q000276:immunology* / Q000503:physiopathology; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology; D050152:Intra-Abdominal Fat; D044140:Receptor, Angiotensin, Type 1; D012307:Risk Factors; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D014661:Vasoconstriction
chemical_list: D016207:Cytokines; D044140:Receptor, Angiotensin, Type 1